The human body is a tremendous complex of chemical, biochemical and physiological processes all being carried on simultaneously. The incredibly complex control of these thousands of chemical and physiological processes is coded into the DNA and RNA of the genes. It is postulated that as people became older and the RNA and DNA and their messages became increasingly "blurred" with time, the control of this enormous complex would begin to lose its ability, among other things, to repair wear and tear.
The body is subject to huge numbers of destructive forces including physical, chemical and biological insults. Among the noxious physical insults is ionizing radiation from many different sources that are completely unavoidable in everyday life. Chemical insults are derived not only from synthetic but from many natural chemicals that are noxious and to which we are exposed. Biological insults are in the form of organisms such as viruses, bacteria and fungi and many of their wastes and noxious products. There is, in sum, a literal barrage of insults which make up our daily environment. It is the repair mechanism which must circumvent these destructive forces. Clearly, if the coded DNA information which controls the repair processes becomes damaged, the stigmata of age will begin.
If you look at the aging process in the last several decades of human life, you can see the repair process is increasingly impaired. Elastic tissue cannot be repaired and wrinkles occur. Muscles and joints can no longer take the punishment of youth. Cancer and other disease-producing agents which are omni-present can no longer be easily rejected. Thus, the body becomes more susceptible to infections, malignant tumors, and a host of other effects of age which, in youth, was of no concern because the body could cope with such everyday challenges.
Coenzyme Q is now generally recognized as an important component of the mitochondrial electron transport processes of respiration and coupled oxidative phosphorylation, and therefore is of fundamental importance to the intracellular energy-producing systems. Evidence has been obtained for the existence of coenzyme Q deficiencies in some pathological processes in: human cardiac, gingival and dystrophic tissues, rats with induced hypertension, mice with hereditary muscular dystrophy, Friend virus induced leukemia and others. The therapeutic application and potential of coenzyme Q was reviewed by Folkers in Iternat. J. Vit. Res. 39:334 (1969) and Cancer Chemoth. Rep. 4:19 (1974).
Coenzyme Q is now among the agents being used experimentally and clinically to enhance nonspecifically the host resistance. In contrast to other materials in use for this purpose, extensive toxicological studies, including those of the New England Institute, revealed no significant abnormalities that would contraindicate the use of coenzyme Q in humans.
Administration of various members of the coenzyme Q family into experimental animals results in increased resistance to a variety of bacterial and protozoal infections, as well as viral and chemical carcinogeneses. It has been postulated that this enhanced resistance is mediated via stimulation of various parameters of the host defense system, a process which has high cellular energy requirement.